Full citation and abstract? Citation:
Talbott, Evelyn O. "Fine particulate matter and the risk of autism spectrum disorder." Environmental Research Volume 140. July (2015): Pages 414-420. Science Direct. Web. 16 Sept 2015. <http://www.sciencedirect.com/science/article/pii/S0013935115001449#>.
Abstract:
The causes of autism spectrum disorder (ASD) are not well known. Recent investigations have suggested that air pollution, including PM2.5, may play a role in the onset of this condition. The objective of the present work was to investigate the association between prenatal and early childhood exposure to fine particulate matter (PM2.5) and risk for childhood ASD. A population-based case-control study was conducted in children born between January 1, 2005 and December 31, 2009 in six counties in Southwestern Pennsylvania. ASD cases were recruited from specialty autism clinics, local pediatric practices, and school-based special needs services. ASD cases were children who scored 15 or above on the Social Communication Questionnaire (SCQ) and had written documentation of an ASD diagnosis. Controls were children without ASD recruited from a random sample of births from the Pennsylvania state birth registry and frequency matched to cases on birth year, gender, and race. A total of 217 cases and 226 controls were interviewed. A land use regression (LUR) model was used to create person- and time-specific PM2.5 estimates for individual (pre-pregnancy, trimesters one through three, pregnancy, years one and two of life) and cumulative (starting from pre-pregnancy) key developmental time periods. Logistic regression was used to investigate the association between estimated exposure to PM2.5 during key developmental time periods and risk of ASD, adjusting for mother's age, education, race, and smoking. Adjusted odds ratios (AOR) were elevated for specific pregnancy and postnatal intervals (pre-pregnancy, pregnancy, and year one), and postnatal year two was significant, (AOR¼1.45, 95% CI¼1.01–2.08). We also examined the effect of cumulative pregnancy periods; noting that starting with pre-pregnancy through pregnancy, the adjusted odds ratios are in the 1.46–1.51 range and significant for pre-pregnancy through year 2 (OR¼1.51, 95% CI¼1.01–2.26). Our data indicate that both prenatal and postnatal exposures to PM2.5 are associated with increased risk of ASD. Future research should include multiple pollutant models and the elucidation of the biological mechanism for PM2.5 and ASD.
Where do the authors work, and what are their areas of expertise? Note any other publications by the authors with relevance to the 6Cities project.
The authors of the journal work at the University of Pittsburgh Graduate School of Public Health. Heinz Endowments funded the work.
The head of the research is Evelyn Talbott, a professor in epidemiology at the Pittsburgh Graduate School of Public Health. Her areas of expertise are environmental and cardiovascular epidemiology. Below are her works related to air pollution:
Vincent C. Arena: Associate Professor of Biostatics at the Pittsburgh Graduate School of Public Health
Judith R. Rager: Department of Epidemiology at the Pittsburgh Graduate School of Public Health
Jane E. Clougherty: Assistant Professor of Environmental and Occupational Health at the Pittsburgh Graduate School of Public Health
Drew R. Micanowicz: Department of Environmental and Occupational Health at the Pittsburgh Graduate School of Public Health
Ravi K. Sharma: Department of Behavioral and Community Health Sciences at the Pittsburgh Graduate School of Public Health
Shaina L. Stacy: Department of Environmental and Occupational Health at the Pittsburgh Graduate School of Public Health
What are the main findings or arguments presented in the article or report?
The main finding of this report is that exposure to PM2.5 prior to, during, and after pregnancy can increase the odds of Autism Spectrum Disorder in children.
Describe at least three ways that the argument is supported.
Used the LUR model and spatial concentration ratios and equations to account for spatial disparities and PM2.5 exposure differences.
For all cases and controls 'average and cumulative exposure estimates' were calculated for 3 months before pregnancy, throughout each trimester, and during their first and second years, in addition to various combinations of the listed time periods.
Found mean total estimated exposure during pregnancy:
"Mean (SD) PM2.5 estimated exposure during pregnancy was 15.0 (1.9) μg/m3 for cases and 14.8 (1.8) for controls. The IQR was 2.80 μg/m3 for cases and 2.84 μg/m3 for controls"
Statistical analysis and significance of effects using:
odds ratios of ASD per 2.84 μg/m3 (IQR) increase in average exposure to PM2.5 (μg/m3 ) during prenatal and postnatal period
odds ratios of ASD per 2.84 μg/m3 (IQR) increase in average exposure to PM2.5 (μg/m3 ) during cumulative developmental periods beginning with pre-pregnancy.
95% Confidence Intervals
All of these tests were conducted from the case/control interquartile range for exposure to PM2.5 (found statistically)
What three (or more) quotes capture the message of the article or report?
"We sought to explore the association between ASD and exposure to PM2.5 during critical prenatal and postnatal periods in a case-control study in the greater Pittsburgh, Pennsylvania."
"Our results showed an approximate 50% increase in risk of ASD associated with an average cumulative exposure from three months before the pregnancy through age two of the child."
"Mean (SD) PM2.5 estimated exposure during pregnancy was 15.0 (1.9) μg/m3 for cases and 14.8 (1.8) for controls. The IQR was 2.80 μg/m3 for cases and 2.84 μg/m3 for controls."
What were the methods, tools and/or data used to produce the claims or arguments made in the article or report?
Cases and controls
ASD cases fit 2 requirements: scored a 15 or above on the Social Communication Questionnaire (SCQ), a screen for the presence of autistic feature and had written documentation, including the Autism Diagnostic Observation Schedule (ADOS) or other diagnostic test results, of a diagnosis of an ASD from a child psychologist or psychiatrist.
Controls required a score below 15 on the SCQ and parent consent; the subjects were chosen randomly from the Pennsylvania Department of Health (PADOH) state birth registry files for 2005 to 2009 in Allegheny, Armstrong, Beaver, Butler, Washington, or Westmoreland County. They were chosen to match ASD cases by birth year, gender, and race.
Measuring PM2.5 exposure
Used ArcGIS to map the residential location of each case/control
In order to estimate the spatial estimation of PM2.5 exposure
Didn't use data from the regional monitors.
Didn't hit all of the areas studied
“do not typically capture a representative range of exposures across urban environments”
"Land use regression (LUR) models were constructed using manual forward step-wise linear regression"
Used regional daily PM2.5 measures from EPA's regulatory Air Quality System (AQS) "to extrapolate the spatial estimates provided by the LUR over the length of study—and to enable exposure estimation at various time scales"
"Daily measures from the AQS site was matched and averaged to our weekly sampling sessions, then substituted for the regional background measures in previously-built seasonal and merged-seasons LURs"
checked the legitimacy of the data
used this information to input to the LUR models
PMij=PMj*[PMi/PMμ]
Allowed calculation of PM2.5
PMi=predicted PM measurement at location i
PMμ= county wide mean PM measurement
[PMi/PMμ]=spatial concentration ratio from LUR model
PMij ="the PM2.5 concentration at location i at time j (24-h concentrations) from the FRM monitor, to calculate daily PM2.5 exposure estimates for all residences and time periods"
How (if at all) are health disparities or other equity issues addressed in the article or report?
Maternal age, paternal age, maternal smoking history (before/during pregnancy), low birth weight and preterm birth were information collected to further analyze the data, by demographic specifics.
Average age of mothers of children with ASD was lower than average age of control children; but the frequency of 40+ maternal age was higher for children with ASD.
Smoking before or during pregnancy occurred in 24.6% of case mothers and 10.5% of control mothers.
23% ASD cases were born low birth weight and 31% preterm.
9% controls were born low birth weight and 20% preterm.
The controls were chosen to match cases in year of birth, gender and race.
This demographic data could have been applied to the analysis of PM2.5 instead of just listed as "data."
Where has this article or report been referenced or discussed? (In some journals, you can see this in a sidebar.)
A response to a collection of studies on links between air pollution and neuropsychological development in children published by the Endocrine Society.
An article on air pollution published by Independent Nurse Select.
This paper is very new but has been cited in legitimate journal papers.
Can you learn anything from the article or report’s bibliography that tells us something about how the article or report was produced?
The study referenced other journals that studied prenatal development.
Declare what is new and better about this experiment
Studied prenatal and postnatal exposure
each alone and then cumulative
Accounted for moving of residents within the 6 counties
Modeling of PM2.5 exposure (LUR model) allowed areas without a nearby monitor to have "more accurate" exposure data.
Other references where used to develop and design the experiment (how to develop a model that was used to develop the method of the LUR; using the data from the EPA's AQS to study pollutant levels).
What three points, details or references from the text did you follow up on to advance your understanding of how air pollution science has been produced and used in governance and education in different settings?
Citation:
Talbott, Evelyn O. "Fine particulate matter and the risk of autism spectrum disorder." Environmental Research Volume 140. July (2015): Pages 414-420. Science Direct. Web. 16 Sept 2015. <http://www.sciencedirect.com/science/article/pii/S0013935115001449#>.
Abstract:
The causes of autism spectrum disorder (ASD) are not well known. Recent investigations have suggested that air pollution, including PM2.5, may play a role in the onset of this condition. The objective of the present work was to investigate the association between prenatal and early childhood exposure to fine particulate matter (PM2.5) and risk for childhood ASD. A population-based case-control study was conducted in children born between January 1, 2005 and December 31, 2009 in six counties in Southwestern Pennsylvania. ASD cases were recruited from specialty autism clinics, local pediatric practices, and school-based special needs services. ASD cases were children who scored 15 or above on the Social Communication Questionnaire (SCQ) and had written documentation of an ASD diagnosis. Controls were children without ASD recruited from a random sample of births from the Pennsylvania state birth registry and frequency matched to cases on birth year, gender, and race. A total of 217 cases and 226 controls were interviewed. A land use regression (LUR) model was used to create person- and time-specific PM2.5 estimates for individual (pre-pregnancy, trimesters one through three, pregnancy, years one and two of life) and cumulative (starting from pre-pregnancy) key developmental time periods. Logistic regression was used to investigate the association between estimated exposure to PM2.5 during key developmental time periods and risk of ASD, adjusting for mother's age, education, race, and smoking. Adjusted odds ratios (AOR) were elevated for specific pregnancy and postnatal intervals (pre-pregnancy, pregnancy, and year one), and postnatal year two was significant, (AOR¼1.45, 95% CI¼1.01–2.08). We also examined the effect of cumulative pregnancy periods; noting that starting with pre-pregnancy through pregnancy, the adjusted odds ratios are in the 1.46–1.51 range and significant for pre-pregnancy through year 2 (OR¼1.51, 95% CI¼1.01–2.26). Our data indicate that both prenatal and postnatal exposures to PM2.5 are associated with increased risk of ASD. Future research should include multiple pollutant models and the elucidation of the biological mechanism for PM2.5 and ASD.
Where do the authors work, and what are their areas of expertise? Note any other publications by the authors with relevance to the 6Cities project.
What are the main findings or arguments presented in the article or report?
Describe at least three ways that the argument is supported.
What three (or more) quotes capture the message of the article or report?
What were the methods, tools and/or data used to produce the claims or arguments made in the article or report?
How (if at all) are health disparities or other equity issues addressed in the article or report?
Where has this article or report been referenced or discussed? (In some journals, you can see this in a sidebar.)
This paper is very new but has been cited in legitimate journal papers.
Can you learn anything from the article or report’s bibliography that tells us something about how the article or report was produced?
What three points, details or references from the text did you follow up on to advance your understanding of how air pollution science has been produced and used in governance and education in different settings?